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Gastroenterology. 1996 Oct;111(4):911-8.

Interleukin 4 acts as an inducer of decay-accelerating factor gene expression in human intestinal epithelial cells.

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Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan.



Decay-accelerating factor (DAF) protects host tissues from the attack of autologous complement activation. In this study, we attempted to define the cytokine regulation of DAF messenger RNA (mRNA) expression in human intestinal epithelial cells.


The effects of cytokines on DAF mRNA accumulation were evaluated by Northern blot analysis. The DAF protein expression was analyzed by both immunoprecipitation and immunoblotting.


Interleukin (IL)-4 induced a marked increase in DAF mRNA accumulation in HT-29 cells. In this line, IL-1 beta evoked only weak induction, and IL-6, IL-8, IL-10, and interferon gamma had no effect. The effect of IL-4 was observed in a dose-dependent manner and confirmed at the protein level. The increase in DAF mRNA accumulation reached a maximum at 3-6 hours and then gradually decreased. These effects of IL-4 on DAF mRNA and protein expression were also observed in T84 cells. The mRNA stability studies suggested that IL-4 regulates DAF gene expression mainly at the transcriptional level.


In human intestinal epithelial cells, IL-4 acts as a potent inducer of DAF mRNA expression, suggesting a cytoprotective role for IL-4 against autologous complement activation.

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